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1.
Abstract

Darifenacin, (S)-2-[1-[2,3-dihydrobenzofuran-5-yl]-3-pyrrolidinyl]-2,2-diphenylacetamide, is a novel muscarinic M3 antagonist. In this study we have compared the binding of [3H]-darifenacin to the five cloned human muscarinic receptors (m1 - m5) expressed in CHO cells. [3H]-darifenacin binds with 6 fold higher affinity to m3 (KD = 0.33 nmol/l) over m1 (KD = 1.6 nmol/l) receptors. There was no specific binding of [3H]-darifenacin to m2 receptors and specific binding to m4 and m5 receptors was insufficient to determine a KD. Binding of [3H]-darifenacin to m1 and m3 was displaced by atropine (m1 pKi = 9.36, m3 pKi = 9.4), 4-DAMP (m1 pKi = 9.04, m3 pKi = 9.19), pirenzepine (m1 pKi = 8.63, m3 pKi = 6.85), methoctramine (m1 pKi = 7.28, m3 pKi = 6.63), and darifenacin (m1 pKi = 8.36, m3 pKi = 9.14), demonstrating that [3H]-darifenacin represents the first selective m3 radioligand.  相似文献   

2.
The antagonist [3H]idazoxan binds with comparable affinity to α2 adrenergic receptors and to phentolamine-displaceable non-stereoselective sites in human frontal cortex membranes. In contrast, idazoxan analogs possessing alkyl and alkoxy substituents at the 2-position of the benzodioxan moiety (i.e. RX 821002: 2-methoxy-1,4-[6,7-3H]benzodioxan-2-yl-2-imidazolin HCl, 43.8 Ci/mmol) possess 300–1200 times lower affinity for the non-stereoselective sites. Their affinity for the α2 receptors is increased as well, resulting in more than a 1000-fold selectivity towards the receptors as compared to the non-stereoselective sites. [3H]RX 821002, the 2-methoxy analog of idazoxan possesses an approx. 10-fold higher affinity for the α2 receptors (KD = 2.8 nM than [3H]idazoxan (KD = 24 nM) and about equal affinity as [3H]rauwolscine (KD = 3.6 nM).[3H]Rauwolscine binds with comparable affinity to α2 receptors and to 5-HT1A receptors, and competition studies indicate that the Ki value of unlabelled RX 821002 for the 5-HT1A receptors (30 nM) is about one order in magnitude above its Ki value for the α2 receptors (4.1 nM). Labelling of the 5-HT1A receptors by [3H]RX 821002 and by [3H]rauwolscine can be prevented by selective masking with 8-OH-DPAT (30 nM) or 5-HT (0.3 μM). Under these conditions, specific binding of [3H]RX 821002 to the α2 receptors represents 84% of total binding (at its KD), as compared to 77% for [3H]rauwolscine and 20% for [3H]idazoxan.[3H]RX 821002 labels the α2 receptors as a single class of non-cooperative sites. Association and dissociation kinetics are very fast at 37°C. Antagonist competition curves are steep with Hill coefficients close to one and the agonist curves can be analysed in terms of two affinity sites, confirming the antagonistic properties of [3H]RX821002. About 60% of the α2 receptors possess high agonist affinity.  相似文献   

3.
G. Le Fur  T. Phan  A. Uzan 《Life sciences》1980,26(14):1139-1148
Direct binding to intact rat lymphocytes has been shown for the potent dopaminergic antagonist [3H]spiroperidol. The specific binding is saturable with two components (KD1 = 1.9 nM, KD2 = 36.2 nM). Determination of the KD by kinetic studies measuring rate constants for association and dissociation provided KD values similar to those obtained in equilibrium experiments. The specific binding is proportional to cell concentration and temperature dependent with a maximum at 37°C. [3H]spiroperidol binding is stereospecific since (+)butaclamol was more effective than (?)butaclamol. The relative potencies of different antidopaminergic agents in competing for [3H]spiroperidol binding sites parallel their activity in the striatum. Dopaminergic receptors have also been demonstrated in other mammalian lymphocytes (rabbit, dog, human). Lymphocyte dopaminergic receptors could be implicated in lymphocytes mediated immune response.  相似文献   

4.
Experiments conducted on membrane fractions of guinea-pig brain using ligand-binding techniques have shown that certain Ca2+-antagonists interact with histamine (H1 or H2) receptors. Flunarizine (inhibition constant, Ki ∼ 86 nM) was nearly as potent as diphenhydramine (Ki ∼ 44 nM) in inhibiting [3H]pyrilamine binding to cerebellar H1-receptors, whereas verapamil, D 600 and nifedipine did not interact with this site. Regarding [3H]tiotidine binding to H2-receptors of cerebral cortex, verapamil (Ki ∼ 1400 nM) and D 600 (Ki ∼ 1240 nM) were nearly as potent as cimetidine (Ki ∼ 910 nM) whereas flunarizine and nifedipine were inactive. The interaction of flunarizine with H1-receptors might explain, in part, its sedative side-effect. The interaction of verapamil with H2-receptors, demonstrated here for the first time, might be involved in the anti-arrhythmic action of this agent.  相似文献   

5.
Properties of [3H]diazepam binding sites on rat blood platelets   总被引:8,自引:0,他引:8  
J K Wang  T Taniguchi  S Spector 《Life sciences》1980,27(20):1881-1888
Intact rat blood platelets are shown to possess benzodiazepine binding sites of the peripheral type, binding of [3H]diazepam being strongly inhibited by Ro5-4864 (Ki = 3.6 ± 0.5 nM) but only weakly inhibited by clonazepam (Ki = 35.1 ± 18.2 μM). Binding of [3H]diazepam is specific and saturable. Scatchard analysis reveals a single class of binding sites with KD = 14.7 ± 1.0 nM and Bmax = 564 ± 75 fmoles/108 platelets. The Hill coefficient is 0.94, indicating a lack of binding site heterogeneity or negative cooperativity. Binding reaches equiliibrium at 6 min, with k+1 = 2.9 × 107 M?1 min?1, and is rapidly reversible (t12 = 2.2 min with K?1 = 0.315 min?1. KD derived from the rate constants agrees with that estimated by Scatchard analysis. KD of the crude membrane fraction of platelets is also close to that of intact platelets. Binding of [3H]diazepam is linear with platelet number (between 0.25–2 × 108 platelets), is temperature sensitive with maximum binding at 0°C, and has a broad optimal pH range between pH 5–9.  相似文献   

6.
[3H]Lysergic acid diethylamide ([3H]LSD) binds on membrane homogenate of honeybee brain to both a dopamine-sensitive site (D-site) and a serotonin-sensitive site (S-site). Under suitable conditions the properties of the two sites can be studied separately. Specific binding of [3H]LSD to both the D-site and the S-site has high affinity and is saturable. The mean equilibrium dissociation constants (KD) were 3.8 nM for the D- and 0.89 nM for the S-site. The densities (Bmax values) of both binding sites were 1.7 pmol/mg protein for the D-site and 0.79 pmol/mg protein for the S-site. [3H]LSD binding to the D-site was reversible and reached equilibrium in about 30 min. Pharmacological displacement studies display a high binding affinity of the putative natural agonist dopamine to the D-site (Ki = 22 nM). The most potent displacers of D-site binding were lisuride, (+)-bromocriptine, chlorpromazine, S(+)-butaclamol, and 6,7-ADTN. The [3H]LSD labelled D-site seems to be G-protein coupled, since addition of the stable GTP analogue GTPγS or NaCl to the incubation medium evoked a decrease of specific [3H]LSD binding to the D-site.  相似文献   

7.
The synthetic peptide octarphin (TPLVTLFK, fragment 12?C19 of ??-endorphin), a selective agonist of the nonopioid ??-endorphin receptor, was labeled with tritium yielding specific activity of 28 Ci/mmol. The binding of [3H]octarphin to rat adrenal cortex membranes was studied under normal conditions as well as after cold and heat shocks. It was found that under normal conditions [3H]octarphin specifically binds to the membranes with high affinity: K d1 = 36.3 ± 2.5 nM, Bmax1 = 41.0 ± 3.8 pmol/mg protein. The specific binding of [3H]octarphin to the membranes was inhibited by unlabeled ??-endorphin (K i = 33.9 ± 3.6 nM) and the agonist of the non-opioid receptor decapeptide immunorphin (K i = 36.8 ± 3.3 nM). Unlabeled naloxone, [Leu5]- and [Met5]enkephalins, ??- and ??-endorphins, and corticotropin were inactive (K i > 1 ??M). Both cold and heat shocks decreased the binding affinity: K d2 = 55.6 ± 4.2 nM and K d3 = 122.7 ± 5.6 nM, respectively. In both cases, the maximal binding capacity of the receptor did not change. Thus, even a short-term thermal shock significantly affects the sensitivity of the non-opioid ??-endorphin receptor of adrenal cortex membranes.  相似文献   

8.
LS‐3‐134 is a substituted N‐phenylpiperazine derivative that has been reported to exhibit: (i) high‐affinity binding (Ki value 0.2 nM) at human D3 dopamine receptors, (ii) > 100‐fold D3 versus D2 dopamine receptor subtype binding selectivity, and (iii) low‐affinity binding (Ki > 5000 nM) at sigma 1 and sigma 2 receptors. Based upon a forskolin‐dependent activation of the adenylyl cyclase inhibition assay, LS‐3‐134 is a weak partial agonist at both D2 and D3 dopamine receptor subtypes (29% and 35% of full agonist activity, respectively). In this study, [3H]‐labeled LS‐3‐134 was prepared and evaluated to further characterize its use as a D3 dopamine receptor selective radioligand. Kinetic and equilibrium radioligand binding studies were performed. This radioligand rapidly reaches equilibrium (10–15 min at 37°C) and binds with high affinity to both human (Kd = 0.06 ± 0.01 nM) and rat (Kd = 0.2 ± 0.02 nM) D3 receptors expressed in HEK293 cells. Direct and competitive radioligand binding studies using rat caudate and nucleus accumbens tissue indicate that [3H]LS‐3‐134 selectively binds a homogeneous population of binding sites with a dopamine D3 receptor pharmacological profile. Based upon these studies, we propose that [3H]LS‐3‐134 represents a novel D3 dopamine receptor selective radioligand that can be used for studying the expression and regulation of the D3 dopamine receptor subtype.  相似文献   

9.
Abstract: The binding of [3H]dopamine to brain regions of calf, rat, and human was investigated. The calf caudate contained the highest density of [3H]dopamine binding sites, with a Bmax value of 185 fmol/mg protein, whereas rat and human striatum contained one-third this number of sites. The KD values for [3H]dopamine in all tissues were 2–3 nM. Dopaminergic catecholamines (dopamine, apomorphine, 6,7-dihydroxy-2-aminotetralin, and N-propylnorapomorphine) inhibited the binding of [3H]dopamine in all three species, at low concentrations, with IC50 values of 1.5 to 6 nM. Neuroleptics, in contrast, inhibited the binding at high concentrations (with IC50 values of 200 to 40,000 nM). The [3H]dopamine binding sites were saturable, heat-labile, and detectable only in dopamine-rich brain regions; these sites differed from D2 dopamine sites (labeled by [3H]butyrophenone neuroleptics), and from Dl dopamine sites (labeled by [3H]thioxanthene neuroleptics) associated with the dopamine-stimulated adenylate cyclase. We have, therefore, called these high-affinity [3H]dopamine binding sites D3 sites. [3H]Apomorphine and [3H]ADTN also appeared to label D3 sites. These ligands however, were less selective than [3H]dopamine, and labeled sites other than D3 as well. Assay conditions were important in determining the parameters of [3H]dopamine binding. The optimum conditions for selective labeling of the D3 dopaminergic sites, using [3H]dopamine, required the presence of EDTA and ascorbate.  相似文献   

10.
[3H]verapamil binding to muscle tubule membrane has the following properties. KD = 27 ± 5 nM and maximum binding capacity Bmax = 50 ± 5 pmol/mg of protein. A 1 = 1 stoichiometry of binding was found for the ratio of [3H]verapamil versus [3H] nitrendipine binding sites. The dissociation constant found at equilibrium is near that determined from the ratio of the rate constants for association (k1) and dissociation (k?1). Antiarrhythmic drugs like D600, diltiazem and bepridil are competitive inhibitors of [3H]verapamil binding with KD values between 40 and 200 nM. Dihydropyridine analogs are apparent non competitive inhibitors of [3H]verapamil binding with half-maximum inhibition values (K0.5) between 1 and 5 nM.  相似文献   

11.
The binding of [3H]SCH 23390 to dopamine (DA) D1-receptors was measured in the nucleus accumbens of rats treated chronically with desipramine for 14 days. DA D1 — and D2-receptor binding using [3H]SCH 23390 and [3H]spiperone, respectively as ligands, was determined in rats treated for 28 days. NeitherB max norK d values were influenced by chronic desipramine treatment. In addition, chronic desipramine treatment (28 days) did not influence the dose dependent, quinpirole (10–1000 nM)-mediated inhibition of the electrically stimulated release of [3H]DA and [14C]ACh from nucleus accumbens slices or the dose dependent increase in [3H]DA release and decrease in [14C]ACh release in the presence of 1 and 10 M nomifensine. Therefore, our results suggest that the effect of chronic antidepressant treatment cannot be attributed to changes in either DA D11-or D2-receptor binding or DA D2-receptor function in the nucleus accumbens.  相似文献   

12.
Using concentrations of [3H] dihydroergokryptine between 0.1 and 5 nM, saturable binding can be demonstrated in rat cerebral cortical membranes with a dissociation constant (KD) of about 0.8 nM. α-Noradrenergic agonists and antagonists compete for the sites labeled by these low concentrations of [3H] dihydroergokryptine with relative potencies characteristics of classical α-noradrenergic receptors. The very low potency of serotonin in competing for these binding sites indicates that, in contrast to findings with higher concentrations of [3H] DHE, low concentrations do not label serotonin receptors. Moreover, the low potency of dopamine in competing for [3H] dihydroergokryptine binding in both striatal and cortical membranes indicates that no detectable portion of binding is associated with postsynaptic dopamine receptors.  相似文献   

13.
Abstract: The binding of radioactive piperidine-4-sulphonic acid ([3H]P4S) to thoroughly washed, frozen, and thawed membranes isolated from cow and rat brains has been studied. Quantitative computer analysis of the binding curves for four regions of bovine brain revealed the general presence of two binding sites. In these brain regions less satisfactory computer fits were obtained for receptor models showing one or three binding sites or negative cooperativity. With the use of Tris-citrate buffer at 0°C the two affinity classes for P4S in bovine cortex membranes revealed the following binding parameters: KD= 17 ± 7 nM (Bmax= 0.15 ± 0.07 pmol/mg protein) and KD= 237 ± 100 nM (Bmax= 0.80 ± 0.20 pmol/mg protein). Heterogeneity was also observed for association and dissociation rates of [3H]P4S. The slow binding component (kon= 5.6 × 107 or 8.8 × 107 M-1 min-1, kOff= 0.83 min-1, and KD= 14.7 or 9.4 nM, determined by two different methods in phosphate buffer containing potassium chloride) corresponds to the high-affinity component of the equilibrium binding curve (KD= 11 nM, Bmax= 0.12 pmol/mg protein in the same buffer system). The association and dissociation rates for the subpopulation of rapidly dissociating sites, apparently corresponding to the low-affinity sites, were too rapid to be measured accurately. The binding of [3H]P4S appears to involve the same two populations of sites with Bmax values similar to those for [3H]GABA binding to the same tissue, although the kinetic parameters for the two ligands are somewhat different. Furthermore, comparative studies on the inhibition of [3H]P4S and [3H]GABA binding by various GABA analogues, strongly suggest that P4S binds to the GABA receptors. The different effects of P4S and GABA on benzodiazepine binding are discussed.  相似文献   

14.
The metabolism of 1α-hydroxyvitamin D3 (1α-OH-D3) was studied in rat liver perfused with [3H]-1α-OH-D3. [3H]-1α-OH-D3 was converted very rapidly to a more polar metabolite, which was identified as 1α,25-dihydroxy-vitamin D3 [1α,25-(OH)2-D3] by co-chromatography with synthetic 1α,25-(OH)2-D3 as well as by gas chromatography-mass spectrometry. [3H]-1α,25-(OH)2-D3 appeared in the perfusate as early as 20 min after addition of [3H]-1α-OH-D3, and its level in the perfusate increased linearly for at least 120 min. These data strongly indicate that 1α-OH-D3 is metabolized to 1α,25-(OH)2-D3, which exerts biological effects on bone and intestine.  相似文献   

15.
Various radioligands have been used to characterize and quantify the platelet P2Y12 receptor, which share several weaknesses: (a) they are metabolically unstable and substrates for ectoenzymes, (b) they are agonists, and (c) they do not discriminate between P2Y1 and P2Y12. We used the [3H]PSB-0413 selective P2Y12 receptor antagonist radioligand to reevaluate the number of P2Y12 receptors in intact platelets and in membrane preparations. Studies in humans showed that: (1) [3H]PSB-0413 bound to 425 ± 50 sites/platelet (KD = 3.3 ± 0.6 nM), (2) 0.5 ± 0.2 pmol [3H]PSB-0413 bound to 1 mg protein of platelet membranes (KD = 6.5 ± 3.6 nM), and (3) competition studies confirmed the known features of P2Y12, with the expected rank order of potency: AR-C69931MX > 2MeSADP ≫ ADPβS > ADP, while the P2Y1 ligand MRS2179 and the P2X1 ligand α,β-Met-ATP did not displace [3H]PSB-0413 binding. Patients with severe P2Y12 deficiency displayed virtually no binding of [3H]PSB-0413 to intact platelets, while a patient with a dysfunctional P2Y12 receptor had normal binding. Studies in mice showed that: (1) [3H]PSB-0413 bound to 634 ± 87 sites/platelet (KD = 14 ± 4.5 nM) and (2) 0.7 pmol ± 0.3 [3H]PSB-0413 bound to 1 mg protein of platelet membranes (KD = 9.1 ± 5.3 nM). Clopidogrel and other thiol reagents like pCMBS or DTT abolished the binding both to intact platelets and membrane preparations. Therefore, [3H]PSB-0413 is an accurate and selective tool for radioligand binding studies aimed at quantifying P2Y12 receptors, to identify patients with P2Y12 deficiencies or quantify the effect of P2Y12 targeting drugs.  相似文献   

16.
l-[3H]Glutamate binding to synaptic plasma membranes from rat cerebral cortices was carried out at 2–4°C in 50 mM Tris-acetate buffer (pH 7.4) using a microfuge centrifugation method. Binding was increased by repeated freezing-thawing and washing in either crude or partially purified synaptic membranes. Scatchard analysis showed a single binding site (dissociation constant, KD = 697 nM; maximal binding capacity, Bmax = 7.5 pmol/mg protein) in four times distilled water washed crude synaptic membrane. After six times freezing-thawing and washing, a new high affinity site (KD1 = 26 nM, Bmax1 = 1.8 pmol/mg protein) appeared and the number of low affinity site was increased with no apparent change in affinity (KD2 = 662 nM, Bmax2 = 10.5 pmol/mg protein). l-[3H]Glutamate binding was inhibited by acidic amino acid analogues that interact with N-methyl-d-aspartate- and quisqualate-sensitive sites of glutamate receptors. Binding was marginally inhibited by kainate and l-2-amino-4-phosphonobutyrate. These results indicate that repeatedly frozen-thawed and washed synaptic plasma membrane is suitable for studying the subtypes and regulation of glutamate receptors.  相似文献   

17.
A high affinity (KD 35 nM) binding site for [3H]cocaine is detected in rat brain Striatum present at 2–3 pmol/mg protein of synaptic membranes. This binding is displaced by cocaine analogues with the same rank order as their inhibition of [3H]dopamine ([3H]DA) uptake into striatal synaptosomes (r = 0.99), paralleling the order of their central stimulant activity. The potent DA uptake inhibitors nomifensine, mazindol, and benztropine are more potent inhibitors of this high affinity [3H]cocaine binding than desipramine and imipramine. Cathinone and amphetamine, which are more potent central stimulants than cocaine, displace the high affinity [3H] cocaine binding stereos-pecifically, but with lower potency (IC50 ~ 1μM) than does cocaine. It is suggested that the DA transporter in Striatum is the putative “cocaine receptor.

Binding of [3H] cocaine, measured in 10 mM Na2HPO4-0.32 M sucrose, pH 7.4 buffer, is inhibited by physiologic concentrations of Na+ and K+ and by biogenic amines. DA and Na+ reduce the affinity of the putative “cocaine receptor” for [3H]cocaine without changing the Bmax, suggesting that inhibition may be competitive. However, TRIS reduces [3H]cocaine binding non-competitively while Na+ potentiates it in TRIS buffer. Binding of [3H]mazindol is inhibited competitively by cocaine. In phosphate-sucrose buffer, cocaine and mazindol are equally potent in inhibiting [3H]mazindol binding, but in TRIS-NaCl buffer cocaine has 10 times lower potency. It is suggested that the cocaine receptor in the striatum may be an allosteric protein with mazindol and cocaine binding to overlapping sites, while Na+ and DA are allosteric modulators, which stabilize a lower affinity state for cocaine.  相似文献   

18.
Abstract: Specific binding of tritiated dopamine, spiperone, and N-propylnorapomorphine was examined in subcellular fractions from bovine caudate nucleus. All fractions contained at least two sets of specific binding sites for [3H]spiperone (KD 1aPP= 0.2 nM, KD 2aPP= 2.2 nM), the higher affinity sites accounting for one-third to one-eighth of the total. [3H]Spiperone binding was slightly enriched over the total particulate fraction in P2, P3, SPM, and a crude fraction of synaptic mitochondria. A microsomal subfraction (P3B2) exhibited the highest specific binding capacity obtained, representing a fourfold enrichment over the total particulate fraction. [3H]Dopamine exhibited apparent binding to a single class of high-affinity sites in all fractions examined (KDaPP= 4.0 nM). A greater than twofold enrichment was observed in all fractions except myelin and P3, with a fivefold enrichment in SPM and P3B2. At least two classes of receptors were labeled by [3H]-N-propylnorapomorphine (KD 1aPP= 0.55 nM, KD 2aPP= 20 nM), using 50 nM-spiperone together with 100 nM-dopamine to define nonspecific binding. Although binding to the higher affinity site was displaced by spiperone, and lower affinity binding by dopamine, comparison of receptor densities with values obtained by using [3H]spiperone and [3H]dopamine directly suggested that [3H]-N-propylnorapomorphine labeled additional sites. We have also examined a postsynaptic membrane (PSM) fraction obtained from SPM by successive extraction with salt and EGTA followed by sonication and separation on a density gradient. [3H]Spiperone binding in PSM was enriched two- to threefold over unfractionated SPM with a concomitant decrease in [3H]dopamine binding. The enrichment in spiperone receptors was almost entirely due to an increase in the number of lower affinity binding sites, suggesting that these sites may be associated with the postsynaptic membrane.  相似文献   

19.
The binding characteristics of the β-adrenergic agonist (±)-[3H]hydroxybenzylisoproterenol to rat adipocyte membranes were studied. Binding was rapid, reaching equilibrium within 10 min at 37°C (second order rate constant k1=1.37·107·M?1·min?1). Dissociation of specific binding by 0.5 mM (?)-isoproterenol suggested dissociation from two different sites with respective dissociation rate constants k2 of 0.106·min?1 and 0.011·min?1.[3H]Hydroxybenzylisoproterenol binding was saturable (Bmax=690±107 fmol/mg protein), yielding curvilinear Scatchard plots. Computer modeling of these data were consistent with the existence of two classes of [3H]hydroxybenzylisoproterenol binding sites, one having high affinity (KD=3.5±0.7 nM) but low binding capacity (10% of the total sites) and one haveing low affinity (KD=101±20 nM) but high binding capacity (90% of the sites). Adrenergic ligands competed with [3H]hydroxybenzylisoproterenol binding with the following order of potency=(?)-propranolol>(?)-isoproterenol>(?)-norepinephrine≈ (?)-epinephrine>>(+)-isoproterenol=(+)-propranolo, which is consistent with binding to β1-adrenergic receptors. Competition curves of [3H]hydroxybenzylisoproterenol binding by the β-agonist (?)-isoproterenol were shallow and modeled to two affinity states of binding, whereas, competition curves by β-antagonist (?)-propranolol were steeper with Hill number near to one. Gpp[NH]p severely reduced [3H]hydroxybenzyl-isoproterenol binding, an effect which apparently resulted from the reduction of the number of both the high and low affinity sites. In membranes which had been previously exposed to (?)-isoproterenol, then number of [3H]hydroxybenzylisoproterenol binding sites was reduced by 50%, an effect which apparently resulted from the loss of part of both the high and low affinity state binding sites. Finally, the ability of (?)-isoproterenol to stimulate adenylate cyclase correlate closely with the ability of (?)-isoproterenol to displace [3H]hydroxybenzylisoproterenol binding. Comparison of these findings with the binding characteristics of the β-antagonist [3H]dihydroalprenolol to rat adipocyte membranes, led to conclude that [3H]hydroxybenzylisoproterenol can be successfully used to label the β-adrenergic receptors of rat fat cells and suggests that it might be a better ligand than [3H]dihydroalprenolol in these cells.  相似文献   

20.
Annemarie Closse 《Life sciences》1983,32(21):2485-2495
[3H]Mesulergine binds with high affinity to rat cerebral cortex membranes. (KD = 1.9 nM, Bmax = 11.3 pM/g tissue). The binding of this ligand is selective for serotonin-2 receptors: Its next highest affinity, which is for dopamine receptors labelled by neuroleptics, is about 50 times weaker than its affinity for serotonin-2 receptors. No significant affinity for serotonin-1, α1-adrenergic or histamine H1 receptors was observed.Specific [3H]mesulergine binding was diminished in the presence of low concentrations of lithium ions.  相似文献   

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